Every year approximately 24,000 patients develop new cancers of the oral cavity. If the larynx and skin are excluded, the oral cavity is the most common site for squamous carcinomas arising in the head and neck. During the past few years experimental evidence has accumulated which indicates that some metabolites of arachidonic acid (C20:4), particularly the primary prostaglandins (PGs), are involved in mechanisms of initiation, promotion, and growth of tumors. Further, manipulation of PG synthesis with analogues and inhibitors will influence the development of tumors. Many physiological and pathophysiological effects formerly attributed to the classical PGs may, in fact, be attributable to the action of other oxygenated metabolites of C20:4 such as mono-and dihydroxylated fatty acids, products of lipoxygenases. At present, virtually nothing is known about the ability of squamous cell carcinomas of the oral cavity to metabolize C20:4 into various cyclo- and lipoxygenase products, simultaneously. The overall objectives of this pilot study are to investigate: (1) the capacity of tumor cell lines, derived from primary oral squamous carcinomas, to produce the primary PGs, 6-keto-PGF1a (permanent metabolite of PGL), TXB2 (permanent metabolite of TXA2), and unsaturated hydroxy fatty acids from C20:4; (2) the effect of select cyclooxygenase and lipoxygenase inhibitors to suppress the formation of C20:4 metabolites in tumor cell lines in culture. After incubation of 14C-C20:4 with oral squamous carcinoma cells in culture, the radioactive metabolites are extracted from cell culture media by means of lipid solvents, then separated, identified, and quantitated by thin layer chromatography (TLC), high pressure liquid chromatography (HPLC), and liquid scintillation counting. The effectiveness of inhibitors of cyclo and lipoxygenases will be determined by establishing dose-response curves for inhibitors and metabolites formed and, accordingly calculating, their IC50.